Disintegrin and metalloproteinase-17 expression level on bleomycin-induced pulmonary fi brosis in rats

Objective To study the expression level of a disintegrin and metalloproteinase-17（ADAM 17） on bleomycin-induced pulmonary fibrosis in rats, investigate the correlation between ADAM17 and transforming growth factor-β1（TGF-β1）, and illustrate the pathogenesis of pulmonary fibrosis. Methods Sixty rats were randomly divided into six groups, 10 in each group. In the control group, the rats were treated with single intratracheal instillation and injected with 0.9% sterile saline solution（5mg/kg）. The model group were divided into 3rd day group, 7th day group, 14 th day group, 21 th day group and 28 th day group. They were all injected with bleomycin（5 mg/kg） and their lung tissues were taken at specified time point respectively. Histological changes of the lung tissues were evaluated by Massson’s stain. The expression of ADAM17 and TGF-β1 proteins was assessed by immunohistochemistry stain and Western blotting, and the expression of their mRNA was detected by reverse transcription-polymerase chain reaction（RT-PCR）. Results Bleomycin-induced pulmonary fibrosis in rats was successfully established, the pathological changes of model groups showed varying degrees of collagen deposition and myofibroblast proliferation. The level of fibrosis in model groups（except the 3rd day group） were higher than those in control group（P＜0.01）. According to immunohistochemistry data, the expressions of TGF-β1 and ADAM17 were higher than those in control group（P＜0.01）, and both of them were the highest in the 14 th day group. The results of Western blotting and RT-PCR were mainly consistent with the immunohistochemical results. Correlation analysis pointed out that TGF-β1 was positively correlated with ADAM17, the correlation coefficients in immunohistochemistry, Western blotting and RT-PCR were 0.777, 0.808, 0.906, respectively（P＜0.01）. Conclusion The expression level of ADAM17 increases in bleomycininduced pulmonary fibrosis in rats, ADAM17 may play the role of inducing pulmonary fibrosis by increasing the expression of TGF-β1.